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KMID : 1140120060110030171
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Cancer Prevention Research
2006 Volume.11 No. 3 p.171 ~ p.175
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Epigenetic Risk Factors of Colorectal Adenoma in Korean
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Yi Kum-Ho
Moon Woo-Chul
Baik Hyun-Wook
Park Ju-Sang
Jang Eun-Jeong
Park Sang-Jong
Park Young-Min
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Abstract
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Cancer developes through the interaction of genetic and environmental factors. Cancer progresses through the accumulation of multiple genetic mutation and epigenetic changes. Diet constituents, by itself or its metabolite, regulate transcription of gene and are related to signal of proliferation, apoptosis, carcinogen metabolism and repair of DNA. Recently, it is known that tumor suppressor gene is inactivated by methylation of CpG island. It is not clear that epigenetic mechanism, especially abnormal methylation of the promoter gene, is related in colorectal adenoma. We investigated the methylene tetrahydrofolate reductase (MTHFR) polymorphism (C677T and A1298C) and methylation of the promoter gene in colorectal adenomatous polyp patients in contrast to control cases with normal mucosa. Test cases (n=14) were diagnosed with colonoscopically confirmed adenomatous polyps in bundang hospital of Seoul National University control cases (n=6) were obtained from bundang jesaeng hospital and with polyp-free by colonoscopy. C667T (28.6% vs 0%) and A1298C (71.4% vs 50%) of MTHFR polymorphisms were more frequent in adenomatous polyp patients. Abnormal methylation of promoter UCHL1 (50% vs 0%), E-CAD (35.7% vs 0%), p16 (21.4% vs 0%), BRCA1 (14.3% vs 0%), MAGE-A
(21.4% vs 0%), GSTP1 (14,.3% vs 0%), DAP kinase (28.57% vs 16.7%) and ppENK (50% vs 33.3%) were more frequent in colorectal polyp patients than in controls. (Cancer Prev Res 11, 171-175, 2006)
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KEYWORD
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Methylene tetrahydrofolate reductase (MTHFR), CpG island, Colon adenoma
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